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Biomedical subjects

E E Daniel

Publications and source records attributed to E E Daniel.

At least 253 records · Page 14Linked to original sources
PubMed1987

Responsiveness of isolated tracheal smooth muscle from normal and sensitized guinea pigs.

Studies of the responsiveness of strips of tracheal smooth muscle and the changes after sensitization of ovalbumin were carried out. The hypothesis that there might be a generalized or a selective change of airway smooth muscle responsiveness to sensitization was examined in vitro. Agonists acting on muscarinic receptors, alpha 1-, alpha 2-, and beta-adrenoceptors, purine receptors, histamine and serotonin receptors, and leukotriene and prostaglandin receptors were tested, as well as mediators released from local nerves by field stimulation and procedures such as elevation of potassium or addition of Ca2+ ionophores which do not involve specific receptors. Sensitivity to serotonin increased significantly in sensitized animals. Total magnitude of the contraction and subsequent relaxation responses to field stimulation also increased significantly. Neither of these changes was large in magnitude. Although there were a few minor changes in sensitivity (pD2) or in maximum responses, the hypothesis of important changes in responses of any sort in tracheal muscle after sensitization was rejected. The question was raised whether this general absence of changed responsiveness in vitro reflected (i) the failure of sensitization to induce generalized smooth muscle hyperresponsiveness, (ii) the loss of the mechanisms of such responsiveness in vitro, or (iii) the inadequacy of in vitro techniques to assess responsiveness present in vivo.

Adenosine↗
PubMed1987

Calcium and contractions of isolated smooth muscle cells from rat myometrium.

Smooth muscle cells were isolated from estrogenized rat myometrium by collagenase digestion. Electron microscopic examination and measurement of cell lengths by image-splitting micrometry were carried out after fixation with acrolein. Mean lengths of cells before and after isolation were 81.7 and 66.9 micron, respectively. Responses of cells were compared with contractions of isolated strips recorded isometrically. Effects of carbachol and KCl were examined in 2 mM Ca, 2 mM Ca + 4 mM EGTA, and 2 mM Ca + 10(-8) M nitrendipine solution. Carbachol and KCl produced concentration-dependent shortening of isolated cells maximal at 30 s after addition. The concentrations of carbachol required to produce shortenings were about 100-fold less than those required to produce isometric contractions; but no major difference was observed in the concentration dependence of cell shortening and isometric contraction produced by potassium-induced depolarization. In 2 mM Ca solution, there was a phasic response, followed by a tonic response such that more than 50% of maximum cell shortening was maintained for 10 min. However, in 2 mM Ca + 4 mM EGTA or 10(-8) M nitrendipine, the tonic contraction was abolished and cells rapidly relaxed after 30 s. If carbachol was added to cells after varying times in the EGTA-containing solution, the ability to initiate a contraction declined exponentially with a half-time of 160 s. Effects of depolarization by KCl were examined in 2 mM Ca plus nitrendipine and 2 mM Ca + 4 mM EGTA solution. Shortening occurred in 2 mM Ca solution by depolarization but not if nitrendipine was added. Though shortening was not observed in 2 mM Ca + 4 mM EGTA solution by KCl, subsequent addition of carbachol induced shortening. These results suggested that there was an intracellular Ca store site from which Ca was released by carbachol and which was not affected by depolarization in the absence of external Ca. No evidence was obtained that the contraction persists in Ca2+-free medium in isolated cells, which is in agreement with previous findings in small muscle strips in which only a similar transient response was obtained.

Animals↗
PubMed1987

Calcium channels in isolated cells and strips of longitudinal muscle of rat myometrium.

The properties of Ca2+ channels in strips and single muscle cells of longitudinal muscle of estrogen-dominated rat myometrium were studied under the effects of elevation of K+ concentration, the partial channel agonist Bay K 8644, and nitrendipine. In isolated strips in 0.5 mM Ca2+, Bay K 8644 (pD2 = 7.8-8.0) lowered the threshold for and enhanced the contractions in response to an elevation of K+ concentration, including the maximum response to K+ elevation alone. Bay K 8644 alone in concentrations up through 10(-6) M did not initiate contractions in 0.5 mM Ca2+ solutions. At higher concentrations (10(-5) M), Bay K 8644 behaved as an antagonist to contractions induced by elevation of K+. In isolated cells 10(-7) M Bay K 8644 enhanced the shortenings to elevated K+ and lowered the threshold K+ concentration required. Also no significant contraction occurred with 10(-7) M Bay K 8644 at normal K+ concentration. In contrast with its effect in isolated strips, no significant increase in maximum shortening (to 60 mM K+) was observed, possibly because cells without a mechanical load were maximally shortened by K+ alone. From these studies, we conclude that Ca2+ channels of isolated strips and cells of rat myometrium behave similarly and have similar properties to those of other smooth muscles in their interactions with elevation of K+, nitrendipine, and Bay K 8644.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1987

Mechanisms of excitatory actions of neurotensin on canine small intestinal circular muscle in vivo and in vitro.

We have shown previously that close intra-arterial injections of neurotensin in vivo inhibited phasic activity induced by field stimulation of the canine small intestine during anaesthesia but had little effect during quiescence. In contrast, in vitro in the present study, full thickness strips of the muscularis externa cut in the circular axis responded to the lowest effective neurotensin concentrations (10(-12) to 10(-9) M) with an increase in frequency and amplitude of spontaneous contractions; as the concentration was increased from 10(-8) to 10(-7) M, neurotensin inhibited spontaneous activity. A small tonic contraction also occurred; it was maximal at 10(-7) M. Since sufficient tetrodotoxin to block field-stimulated nerve responses did not significantly reduce any of these responses in vitro, the neurotensin responses in vitro did not appear to involve actions on nerves. Indomethacin did not alter the excitatory response to 10(-11) M neurotensin but 5,8,11,14-eicosatetraynoic acid inhibited the excitatory response in a reversible fashion, without altering the response to acetylcholine. Thus excitation in vitro may require the release of excitatory metabolites of arachidonic acid via the lipoxygenase pathway. The neurotensin response in vivo was further studied by evaluating its actions against repetitive submaximal contractions induced by intra-arterial injections of acetylcholine given every minute. Doses that produced a short inhibition of the field-stimulated activity (10(-11) to 10(-10) mol intra-arterially) did not produce inhibition but 10(-10) mol significantly increased the response to acetylcholine. Higher doses (10(-9) mol) produced a significant inhibition of the first subsequent acetylcholine dose but no enhancement of later doses.(ABSTRACT TRUNCATED AT 250 WORDS)

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1987

Structural effects of exposure of smooth muscle in sucrose gap apparatus.

Structural changes were studied over time of a smooth muscle tissue (opossum esophagus circular muscle) exposed in various compartments of a functioning single sucrose gap. The tissues in the Krebs-perfused compartment were qualitatively normal, possessing nerve profiles with little damage, normal appearing smooth muscle and interstitial cells of Cajal as well as gap junctions between muscle cells and interstitial cells. However, in the sucrose compartment tissues had serious damage to smooth muscle, interstitial cells and nerves, and normal gap junctions disappeared. There was also damage to all these structures in tissues exposed to KCl, but most striking was the disappearance of most interstitial cells. These studies raise serious questions about the assumptions underlying the basis for functioning of multicellular tissues in the sucrose gap.

Animals↗
PubMed1987

Corelease of PHI and VIP by vagal stimulation in the dog.

Electrical vagal stimulation increased immunoreactive peptide histidine isoleucine (IR-PHI) and vasoactive intestinal polypeptide (IR-VIP) levels in the portal plasma in anesthetized dogs, depending on the stimulation frequency. Atropine failed to suppress the vagal release of IR-PHI and IR-VIP, whereas hexamethonium abolished the increase of both peptide immunoreactivities. Gel filtration profiles of IR-PHI and IR-VIP in the portal plasma obtained during vagal stimulation revealed major peaks of IR-PHI and IR-VIP eluting in the same positions as synthetic PHI-27 and VIP-28, respectively. These data demonstrate that PHI and VIP are coreleased by vagal stimulation via a nicotinic ganglionic mechanism. An additional peak of larger molecular weight IR-PHI was observed in gel filtration of the portal plasma obtained under higher frequency vagal stimulation, when measured by the N-terminal-specific PHI antiserum. The presence of this larger form of IR-PHI together with a PHI-27-like component was also demonstrated in tissue extracts of the entire length of the gastrointestine, particularly in higher concentration in the stomach. The structure and the physiological significance of this larger form of IR-PHI remains to be elucidated.

Animals↗
PubMed1987

Exogenous opiates: their local mechanisms of action in the canine small intestine and stomach.

Methionine-enkephalin (Met-Enk) and dynorphin were injected intra-arterially into the distal stomach and small intestine of the anesthetized dog during quiescence and phasic activity initiated by field stimulation or intra-arterially administered motilin. The effects of morphine, [D-Ala2, N-Me-Phe4, Met(O)5-ol]enkephalin (Met-ol), and [D-Ala2, D-Leu5]enkephalin (DADLE) were also examined. Opiates had no effect on the quiescent stomach but produced inhibition of phasic contractions (potencies: dynorphin greater than Met-Enk greater than Met-ol greater than DADLE greater than morphine). In the quiescent small intestine, low doses of each opiate, except dynorphin, produced excitation (potencies: Met-Enk congruent to Met-ol congruent to DADLE greater than morphine). Excitation apparently occurred via release of acetylcholine and a partially naloxone-sensitive direct stimulation of smooth muscle. During phasic activity all opiates produced inhibition of phasic muscular contractions (relative potencies as in the stomach). Inhibition by dynorphin in both the stomach and small intestine was shown to occur via naloxone-sensitive inhibition of release of acetylcholine from nerves. Thus inhibition by opiates appears common to the stomach and small intestine, and excitation is a function of opiate action only in the small intestine. Dynorphin may be a natural neuropeptide causing inhibition, and Met-Enk may be a natural neuropeptide causing excitation.

Animals↗
PubMed1987

Activation of endogenous excitatory opiate pathways in canine small intestine by field stimulation and motilin.

Field stimulation of intrinsic nerves (40 V, 0.5 ms, 1-5 pps for 3-10 min) or intraarterial administration of motilin (10(-11)-10(-8 mol) caused contractions of the canine small intestine that were partially resistant to atropine and abolished by tetrodotoxin. Naloxone (10 micrograms ia or 200 micrograms/kg iv) in selective doses (10(-10)-10(-9) mol) that left responses to intra-arterial acetylcholine unaffected reduced responses to field stimulation or motilin in the ileum in the absence of atropine or residual responses in the presence of atropine. Results in the jejunum were similar except that selective doses of naloxone (10 micrograms ia or 200 micrograms/kg iv) increased the sensitivity to motilin in the absence of atropine. Higher doses of naloxone decreased these responses. In common with naloxone, tachyphylaxis to methionine-enkephalin (Met-Enk) reduced the responses to field stimulation or motilin before or after atropine but did not affect the responses to acetylcholine before or the responses to field stimulation of muscle after atropine. These findings are consistent with the hypothesis that Met-Enk may be a noncholinergic, excitatory transmitter released by field stimulation of nerves or intra-arterial motilin in the canine intestine.

Animals↗
PubMed1987

Airway responsiveness to methacholine during the natural menstrual cycle and the effect of oral contraceptives.

Exacerbations of symptoms have been reported in some women with asthma just prior to and during menstruation. We examined changes in airway responsiveness to methacholine during 2 consecutive menstrual cycles in 17 well-controlled asthmatics with a wide range of airway responsiveness. In 10 women with regular natural cycles, measurements were made 1 wk before and 1 wk after the start of menstruation to coincide with the highest and lowest progesterone levels. The mean concentration of methacholine to cause a fall in FEV1 of 20% (PC20) premenstruation was 1.49 mg/ml, which was not significantly different from the mean postmenstruation PC20 of 1.34 mg/ml (p = 0.45). Although there were only 10 subjects, the power was 96%, indicating little likelihood of any difference between the 2 phases. In 7 women taking oral contraceptives, the mean PC20, measured within 1 wk of completing a 21-day course, was 1.19 mg/ml, which was not different from the mean PC20 of 0.97 mg/ml measured after the start of menstruation but before restarting medication (p = 0.17). The power was 98%. In both groups, there was no difference in FEV1 or medication use during the cycle, but symptoms were worse during menstruation. The results suggest that the fluctuations in serum progesterone levels that occur during natural menstrual cycles are insufficient to alter airway responsiveness in an unselected sample of asthmatic women. They also demonstrate that changes in symptoms occur during the cycle both in women with natural cycles and those using contraceptives and that these changes are not related to serum progesterone levels or airway responsiveness.

Adult↗
PubMed1987

The role of substance P in the human urinary bladder.

Detrusor muscle from human bladder contracted to field stimulation after atropine. It also responded to exogenous substance P by an atropine-insensitive mechanism. We tested whether substance P might mediate noncholinergic excitation. Tachyphylaxis to substance P did not effect noncholinergic responses to field stimulation. A substance P antagonist was ineffective in blocking responses to field stimulation or to exogenous substance P. Capsaicin had only nonspecific depressant effects on field stimulated contraction in high (10(-4) M) concentrations. These data do not support the hypothesis that substance P is the mediator of noncholinergic, field stimulated contractions of human detrusor muscle.

Atropine↗
PubMed1987

Pathophysiology of genetic and experimental hypertension.

Evidence is summarized that some structural changes in resistance arteries (hyperplasia of smooth muscle and others) precede the development of vessel changes in genetic hypertension. Additional changes, such as hypertrophy of vascular muscle and altered collagen and elastin, accompany hypertension and contribute to its maintenance. Furthermore, some membrane defects, including reduced Ca2+-pumping by sarcolemma of vascular smooth muscle, contribute to the causation of genetic and experimental hypertension, as well as to some changes in hypertension associated with volume expansion. Analysis of these causative factors may aid in treatment and, ultimately, allow the prevention of hypertension.

Animals↗
PubMed1987

Beta adrenoreceptor in vascular smooth muscle with special reference to subcellular localization and number of binding sites.

The binding of monoiodinated cyanopindolol (ICYP) to membranes from canine and rat aortas, mesenteric arteries and mesenteric nerves has been studied. Binding of ICYP was shown by differential centrifugation and sucrose gradient purification as well as digitonin treatment to be directly related to the content of arterial muscle plasma membrane assessed by marker enzymes. The Kd values obtained were all in the range of 10 to 30 pM but maximum binding site (Bmax) values varied depending upon the extent of contamination by nonplasmalemmal membranes. The more purified plasma membrane fractions have Bmax many times higher than those reported in the literature. Although purified membrane fractions all had ICYP binding characterized by a single binding site with similar Kd values, binding to some crude fractions was complex. In addition, plasma membranes for mesenteric nerves, removed carefully by dissection in our study, were shown to contain ICYP binding sites with a similar Kd and Bmax values to those in arterial muscle membrane. Using arterial muscle purified membranes after removal of nerves by dissection, Bmax values from mesenteric arteries were demonstrated to be much larger than those from aorta in both species. Although the necessity of purifying the membranes depends on the objectives of a given experiment, our result strongly suggest that measurement of changes in receptor densities requires an analytical approach which provides plasma membrane-enriched fractions derived from a single cell type and purified to a known and comparable degree, especially when changes in density related to experimental or disease processes are being investigated.

Animals↗
PubMed1987

The action of trimebutine maleate on gastrointestinal motility is mediated by opiate receptors in human subjects.

The effects of trimebutine on interdigestive motor activity of the small intestine and the colon were studied in healthy volunteers. Trimebutine induced in all subjects phase III-like motor complexes, which were similar to spontaneously occurring phase III complexes of the interdigestive cycle in antrum and duodenum. Trimebutine-induced complexes were suppressed by naloxone. Trimebutine and/or naloxone had no consistent effect on interdigestive contractile activity in the colon.

Adult↗
PubMed1987

Local actions of trimebutine on canine gastrointestinal tract.

The local actions of trimebutine on the circular muscle of canine gastrointestinal tract were studied after close intraarterial injection. The effects resembled those of metenkephalin at all sites. In stomach, trimebutine had no excitatory effects, but inhibited responses mediated by cholinergic post-ganglionic nerves. In small intestine, trimebutine stimulated the quiet gut by probably both neural and direct smooth muscle mechanisms, and it inhibited the field-stimulated phasic contractions. In large intestine, trimebutine had no excitatory actions and only weak inhibitory actions on the field-stimulated gut. Excitatory actions most likely seem to use the mu or delta receptors while inhibitory actions may focus on kappa opiate receptors.

Animals↗
PubMed1987

Frequency analysis of gut EMG.

The EMG of the gut smooth muscle plays an important role in the regulation of gastrointestinal motility in health and disease. The EMG in general consists of an omnipresent oscillatory electrical control activity (ECA) and spikes or other potentials that result in contractions of the smooth muscle. This paper addresses the question of how the ECA signals can best be processed and how inappropriate transformations of such signals may produce misleading results. The various factors affecting the composition of the gut EMG, in time and space along the gut, are discussed briefly. The need for the analysis of the ECA for its oscillatory nature is mentioned together with details regarding the widely used visual, period, and Fourier analysis techniques. Fourier analysis techniques have been applied with increasing frequency to gut EMG; the various features of Fourier analysis and considerations for their implementation on the computer are discussed. The visual, period, and Fourier analysis approaches as well as their uses and limitations in application to a variety of ECAs of the stomach and of the colon in dogs and humans are illustrated. This study indicates that period analysis techniques are well suited for the study of the visibly oscillatory upper gut EMG, while smoothed spectral analysis is more appropriate for the study of colonic EMG.

Animals↗
PubMed1986

Control of human colonic motor function.

Human colonic motility is governed by control mechanisms involving the electrical activity of the smooth muscle cell membranes, the intrinsic and extrinsic nervous activity, and hormonal action. The structural bases for neural and myogenic control have not been demonstrated. However, gap junctions are lacking between muscle cells, and nerves are not close to smooth muscle cells. The myogenic control, as observed in vitro, is described and compared with results obtained from different in vivo techniques. In vitro and in vivo measurements are critically evaluated, and a reconciliation between them attempted. No appropriate animal model is available to help resolve different findings and interpretations. Neural control of colon motility is exerted probably through modulation of myogenic activity as well as directly. The activities of extrinsic nerves, intrinsic motor nerves and afferent nerves are integrated within the colon, at prevertebral ganglia and in the spinal cord in animals, but similar data are not available for the human. There is a lack of studies directly relating transit to motility and conventional beliefs need reexamination.

Animals↗
PubMed1986

Comparison of methodologies for the measurement of antroduodenal motor activity in the dog.

We have compared the abilities of intraluminal strain gauges and manometry to record motor activity from the antrum and duodenum of the anesthetized dog. Responses to intraarterial carbachol, vagal stimulation, and field stimulation recorded by these devices were compared to those registered by strain gauges sewn onto the overlying serosa. In the antrum, the perfused tube (PT) recorded 98% and 97% of field- and vagal-stimulated phasic contractions, respectively, compared with 83% and 90% (p less than 0.005) registered by the intraluminal tube-mounted strain gauges (TSGs). In contrast, in the duodenum there was no difference between the accuracy of these devices in recording phasic activity induced by field stimulation (PT 90% and TSG 87%). Similarly, there was no difference between the abilities of these devices to record tonic contraction induced by carbachol in the antrum (PT 87% and TSG 90%) or duodenum (PT 82% and TSG 87%). However, TSGs misrepresented the configuration of phasic or tonic contractions, producing bifid, negative, or biphasic contractions substantially more frequently than did PT (p less than 0.005). These results illustrate that the accuracy of these two commonly used techniques may be influenced by anatomic factors as well as by the type of contraction recorded.

Animals↗